Yu X, Lin S, Wang X
Guangdong Provincial Cardiovascular Institute, Guangzhou 510080.
Zhonghua Yi Xue Za Zhi. 1999 Apr;79(4):264-7.
To investigate the alteration in steady-state levels of messenger RNA(mRNA) of beta-adrenoceptor signal transmitters in heart failure.
The reverse transcription polymerase chain reaction (RT-PCR) was used to assess gene expression in small quantity of circulatory lymphocytes. With selected oligonucleotide primers, we used quantitative RT-PCR to amplify mRNAs encoding beta 2-adrenergic receptor(beta 2-AR), adenylate cyclase (AC), beta 2-adrenergic receptor kinase(beta-ARK), and beta-arrestin and cAMP response element binding protein (CREB) in 16 healthy subjects and 30 heart-failing patients.
The alteration of gene expression in heart failure appeared to be selective, the steady-state levels of mRNA increased significantly involving AC and the transcription factor, CREB; decreased significantly involving membrane receptor, beta 2-AR; unchanged significantly involving phosphorylating factors of beta-AR uncoupling, beta-ARK and beta-arrestin.
The aberrant gene expression of beta-adrenergic receptor might play an important role in the pathogenesis of heart failure.
研究心力衰竭时心脏β-肾上腺素能受体信号转导分子信使核糖核酸(mRNA)稳态水平的变化。
采用逆转录聚合酶链反应(RT-PCR)技术检测少量循环淋巴细胞中的基因表达。选用寡核苷酸引物,运用定量RT-PCR技术扩增16例健康受试者和30例心力衰竭患者中编码β2-肾上腺素能受体(β2-AR)、腺苷酸环化酶(AC)、β2-肾上腺素能受体激酶(β-ARK)、β-抑制蛋白以及环磷酸腺苷反应元件结合蛋白(CREB)的mRNA。
心力衰竭时基因表达变化具有选择性,AC及转录因子CREB的mRNA稳态水平显著升高;膜受体β2-AR的mRNA稳态水平显著降低;β-AR解偶联磷酸化因子β-ARK和β-抑制蛋白的mRNA稳态水平无明显变化。
β-肾上腺素能受体基因表达异常可能在心力衰竭发病机制中起重要作用。